ArticleBMC developmental biology2006
Increased large conductance calcium-activated potassium (BK) channel expression accompanied by STREX variant downregulation in the developing mouse CNS.
Article in BMC developmental biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed.
- Human Foetal Neuroblasts Exhibit BK Channel-Dependent Membrane Voltage Oscillations upon Depolarization.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
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- Large conductance voltage-and calcium-activated KFrontiers in pharmacology · 2024Review
- Novel Thioxothiazolo[3,4-ACS medicinal chemistry letters · 2022Article
- An emerging spectrum of variants and clinical features inChannels (Austin, Tex.) · 2021Review
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- Article
- Article
- BK Channels in the Central Nervous System.International review of neurobiology · 2016Review
- Age-related changes in nicotine response of cholinergic and non-cholinergic laterodorsal tegmental neurons: implications for the heightened adolescent susceptibility to nicotine addiction.Neuropharmacology · 2014Article
- Article
- Ca(2+)-dependent large conductance K(+) currents in thalamocortical relay neurons of different rat strains.Pflugers Archiv : European journal of physiology · 2013Article
- Article
- Behavioral characterization of cereblon forebrain-specific conditional null mice: a model for human non-syndromic intellectual disability.Behavioural brain research · 2012Article
- Functional upregulation of Ca(2+)-activated K(+) channels in the development of substantia nigra dopamine neurons.PloS one · 2012Article
- Intragenic alternative splicing coordination is essential for Caenorhabditis elegans slo-1 gene function.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Alternatively spliced domains interact to regulate BK potassium channel gating.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Identification and quantification of full-length BK channel variants in the developing mouse cochlea.Journal of neuroscience research · 2011Article
- Upregulation of STREX splice variant of the large conductance Ca2+-activated potassium (BK) channel in a rat model of mesial temporal lobe epilepsy.Neuroscience research · 2011Article
- Intron retention facilitates splice variant diversity in calcium-activated big potassium channel populations.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
Corrections and comments
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4 authors.
Funding
Abstract
backgroundLarge conductance calcium- and voltage activated potassium (BK) channels are important determinants of neuronal excitability through effects on action potential duration, frequency and synaptic efficacy. The pore- forming subunits are encoded by a single gene, KCNMA1, which undergoes extensive alternative pre mRNA splicing. Different splice variants can confer distinct properties on BK channels. For example, insertion of the 58 amino acid stress-regulated exon (STREX) insert, that is conserved throughout vertebrate evolution, encodes channels with distinct calcium sensitivity and regulation by diverse signalling pathways compared to the insertless (ZERO) variant. Thus, expression of distinct splice variants may allow cells to differentially shape their electrical properties during development. However, whether differential splicing of BK channel variants occurs during development of the mammalian CNS has not been examined.
resultsUsing quantitative real-time polymerase chain reaction (RT-PCR) Taqmantrade mark assays, we demonstrate that total BK channel transcripts are up regulated throughout the murine CNS during embryonic and postnatal development with regional variation in transcript levels. This upregulation is associated with a decrease in STREX variant mRNA expression and an upregulation in ZERO variant expression.
conclusionAs BK channel splice variants encode channels with distinct functional properties the switch in splicing from the STREX phenotype to ZERO phenotype during embryonic and postnatal CNS development may provide a mechanism to allow BK channels to control distinct functions at different times of mammalian brain development.
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